We have been pursuing the changes in lipid metabolism that occur when platelets aggregate. We have recently been examining three areas: (1) The specific activation of phospholipases during thrombin-induced aggregation. Oleic acid incorporation into lecithin in intact platelets is stimulated, but palmitic, stearic, eicosatrienoic, and arachidonic acid incorporation is inhibited by thrombin. Linoleic acid uptake into total lecithin seems not to be altered. Incorporation of all fatty acids into triglycerides is virtually abolished. We wish to define the subcellular location of the affected phospholipases and to examine the structural basis for the observed effects. (2) We have also been looking at the synthesis and release of prostaglandins. Platelets are active in PG synthesis and release and are at the same time strikingly sensitive to the presence of exogenous PG's. They afford a readily available, pure tissue for study of the intermediate steps of PG formation and release. (3) Another are of interest is to define the significance of the marked increase in PI synthesis that occurs in platelets as they aggregate. Whether the processes are similar to those that occur in neurosecretory tissue and in phagocytotic cells remians to be explored.